NSG 3280 Pathophysiology Exam 3 Review Actual Exam
2026/2027: Complete Exam-Style Questions with
Detailed Rationales | 100% Verified | Pass Guaranteed –
A+ Graded
TABLE OF CONTENTS
Section 1 | Endocrine Disorders | Q1 – Q10
Section 2 | Neurological Disorders | Q11 – Q20
Section 3 | Musculoskeletal Pathophysiology | Q21 – Q30
Section 4 | Gastrointestinal and Hepatobiliary Disorders | Q31 – Q40
Section 5 | Renal and Genitourinary Pathophysiology | Q41 – Q50
Instructions: Choose the single best answer. Pass: 80% in 90 minutes.
══════════════════════════════════════
SECTION 1: ENDOCRINE DISORDERS Q1 – Q10
══════════════════════════════════════
Question 1 of 50
A 22-year-old patient with type 1 diabetes presents to the emergency department with a
blood glucose of 520 mg/dL, pH 7.28, and positive serum ketones. The patient reports
polyuria, polydipsia, and fruity breath odor over the past 36 hours.
A. Insulin deficiency has led to uncontrolled lipolysis and ketone body production from
free fatty acids.
B. Absolute insulin deficiency has caused hyperglycemia, osmotic diuresis, and
ketogenesis due to unrestrained glucagon and counter-regulatory hormone activity. ✓
CORRECT
C. The patient has developed insulin resistance at the cellular level, causing glucose to
accumulate in the bloodstream.
D. Exogenous insulin has triggered an autoimmune response that destroys pancreatic
beta cells and releases ketones.
,Correct Answer: B
Rationale: In type 1 diabetes, absolute insulin deficiency removes the brake on glucagon
and catecholamines, driving hepatic ketogenesis and hyperglycemia simultaneously.
Insulin resistance is the defining mechanism of type 2 diabetes, not type 1. Exogenous
insulin does not cause autoimmune beta cell destruction; the autoimmune process is
the underlying cause of the insulin deficiency itself.
Question 2 of 50
A 34-year-old patient with untreated Graves disease develops a temperature of 104°F,
severe tachycardia, agitation, and vomiting after a respiratory infection. The patient is
diaphoretic and confused.
A. The patient is experiencing a hypothyroid crisis caused by excessive thyroid hormone
destruction.
B. The patient has developed Hashimoto thyroiditis with acute lymphocytic infiltration of
the gland.
C. The symptoms are consistent with myxedema coma triggered by excessive iodine
intake.
D. The patient is in thyroid storm, a life-threatening hypermetabolic state caused by
abrupt release of stored thyroid hormone and increased peripheral conversion of T4 to
T3. ✓ CORRECT
Correct Answer: D
Rationale: Thyroid storm is characterized by extreme hypermetabolism from massive
thyroid hormone release and increased T3 conversion, often precipitated by infection or
stress. Hypothyroid crisis and myxedema coma present with hypothermia and
bradycardia, the opposite of this presentation. Hashimoto thyroiditis is an autoimmune
hypothyroid condition and does not cause acute hypermetabolic crisis.
Question 3 of 50
,A 58-year-old patient reports fatigue, weight gain, constipation, and cold intolerance
over the past 8 months. Laboratory studies show a TSH of 18.5 mIU/L and a free T4 of
0.6 ng/dL.
A. Primary hypothyroidism is present because the thyroid gland is unable to produce
adequate T4, causing the pituitary to release excess TSH in a compensatory feedback
loop. ✓ CORRECT
B. Secondary hypothyroidism is present because the pituitary is overproducing TSH and
suppressing thyroid function.
C. The patient has subclinical hyperthyroidism with an elevated TSH masking underlying
thyrotoxicosis.
D. The low free T4 indicates iodine deficiency alone without any glandular dysfunction.
Correct Answer: A
Rationale: Elevated TSH with low free T4 defines primary hypothyroidism, where the
thyroid gland fails and the pituitary increases TSH to stimulate hormone production.
Secondary hypothyroidism would show low or inappropriately normal TSH, not elevated.
Subclinical hyperthyroidism presents with low TSH, and iodine deficiency alone does
not explain the marked TSH elevation and classic symptom cluster.
Question 4 of 50
A 45-year-old patient with a pituitary adenoma presents with central obesity, purple
striae on the abdomen, proximal muscle weakness, and a fasting glucose of 180
mg/dL.
A. The patient has primary adrenal insufficiency with destruction of the adrenal cortex
by autoimmune antibodies.
B. The patient is experiencing pheochromocytoma with episodic catecholamine release
causing metabolic syndrome.
C. Excess ACTH from the pituitary adenoma drives bilateral adrenal hyperplasia and
cortisol overproduction, producing Cushing disease. ✓ CORRECT
D. The patient has Conn syndrome with aldosterone excess causing sodium retention
and striae formation.
, Correct Answer: C
Rationale: A pituitary adenoma secreting ACTH causes Cushing disease, which
stimulates the adrenal cortex to overproduce cortisol and creates the classic phenotype
of central obesity, striae, and hyperglycemia. Primary adrenal insufficiency causes
cortisol deficiency, not excess. Pheochromocytoma causes hypertension and sweating,
not striae. Conn syndrome produces hypertension and hypokalemia from aldosterone
excess without cushingoid features.
Question 5 of 50
A 38-year-old patient with autoimmune adrenalitis presents with hypotension,
hyponatremia, hyperkalemia, and hyperpigmentation of the skin creases and oral
mucosa.
A. The patient has secondary adrenal insufficiency from chronic exogenous
corticosteroid use.
B. Autoimmune destruction of the adrenal cortex has caused aldosterone and cortisol
deficiency, leading to sodium loss, potassium retention, and ACTH-driven melanocyte
stimulation. ✓ CORRECT
C. The patient has a pheochromocytoma causing episodic catecholamine release and
electrolyte disturbances.
D. Excess cortisol production from an adrenal adenoma has suppressed the
hypothalamic-pituitary axis.
Correct Answer: B
Rationale: Primary adrenal insufficiency from autoimmune adrenalitis destroys cortisol
and aldosterone production, causing hypotension, hyponatremia, and hyperkalemia,
while elevated ACTH stimulates skin hyperpigmentation. Secondary adrenal
insufficiency lacks hyperpigmentation and mineralocorticoid deficiency because ACTH
is low. Pheochromocytoma and excess cortisol syndromes do not present with
hypotension and hyperpigmentation.
Question 6 of 50
2026/2027: Complete Exam-Style Questions with
Detailed Rationales | 100% Verified | Pass Guaranteed –
A+ Graded
TABLE OF CONTENTS
Section 1 | Endocrine Disorders | Q1 – Q10
Section 2 | Neurological Disorders | Q11 – Q20
Section 3 | Musculoskeletal Pathophysiology | Q21 – Q30
Section 4 | Gastrointestinal and Hepatobiliary Disorders | Q31 – Q40
Section 5 | Renal and Genitourinary Pathophysiology | Q41 – Q50
Instructions: Choose the single best answer. Pass: 80% in 90 minutes.
══════════════════════════════════════
SECTION 1: ENDOCRINE DISORDERS Q1 – Q10
══════════════════════════════════════
Question 1 of 50
A 22-year-old patient with type 1 diabetes presents to the emergency department with a
blood glucose of 520 mg/dL, pH 7.28, and positive serum ketones. The patient reports
polyuria, polydipsia, and fruity breath odor over the past 36 hours.
A. Insulin deficiency has led to uncontrolled lipolysis and ketone body production from
free fatty acids.
B. Absolute insulin deficiency has caused hyperglycemia, osmotic diuresis, and
ketogenesis due to unrestrained glucagon and counter-regulatory hormone activity. ✓
CORRECT
C. The patient has developed insulin resistance at the cellular level, causing glucose to
accumulate in the bloodstream.
D. Exogenous insulin has triggered an autoimmune response that destroys pancreatic
beta cells and releases ketones.
,Correct Answer: B
Rationale: In type 1 diabetes, absolute insulin deficiency removes the brake on glucagon
and catecholamines, driving hepatic ketogenesis and hyperglycemia simultaneously.
Insulin resistance is the defining mechanism of type 2 diabetes, not type 1. Exogenous
insulin does not cause autoimmune beta cell destruction; the autoimmune process is
the underlying cause of the insulin deficiency itself.
Question 2 of 50
A 34-year-old patient with untreated Graves disease develops a temperature of 104°F,
severe tachycardia, agitation, and vomiting after a respiratory infection. The patient is
diaphoretic and confused.
A. The patient is experiencing a hypothyroid crisis caused by excessive thyroid hormone
destruction.
B. The patient has developed Hashimoto thyroiditis with acute lymphocytic infiltration of
the gland.
C. The symptoms are consistent with myxedema coma triggered by excessive iodine
intake.
D. The patient is in thyroid storm, a life-threatening hypermetabolic state caused by
abrupt release of stored thyroid hormone and increased peripheral conversion of T4 to
T3. ✓ CORRECT
Correct Answer: D
Rationale: Thyroid storm is characterized by extreme hypermetabolism from massive
thyroid hormone release and increased T3 conversion, often precipitated by infection or
stress. Hypothyroid crisis and myxedema coma present with hypothermia and
bradycardia, the opposite of this presentation. Hashimoto thyroiditis is an autoimmune
hypothyroid condition and does not cause acute hypermetabolic crisis.
Question 3 of 50
,A 58-year-old patient reports fatigue, weight gain, constipation, and cold intolerance
over the past 8 months. Laboratory studies show a TSH of 18.5 mIU/L and a free T4 of
0.6 ng/dL.
A. Primary hypothyroidism is present because the thyroid gland is unable to produce
adequate T4, causing the pituitary to release excess TSH in a compensatory feedback
loop. ✓ CORRECT
B. Secondary hypothyroidism is present because the pituitary is overproducing TSH and
suppressing thyroid function.
C. The patient has subclinical hyperthyroidism with an elevated TSH masking underlying
thyrotoxicosis.
D. The low free T4 indicates iodine deficiency alone without any glandular dysfunction.
Correct Answer: A
Rationale: Elevated TSH with low free T4 defines primary hypothyroidism, where the
thyroid gland fails and the pituitary increases TSH to stimulate hormone production.
Secondary hypothyroidism would show low or inappropriately normal TSH, not elevated.
Subclinical hyperthyroidism presents with low TSH, and iodine deficiency alone does
not explain the marked TSH elevation and classic symptom cluster.
Question 4 of 50
A 45-year-old patient with a pituitary adenoma presents with central obesity, purple
striae on the abdomen, proximal muscle weakness, and a fasting glucose of 180
mg/dL.
A. The patient has primary adrenal insufficiency with destruction of the adrenal cortex
by autoimmune antibodies.
B. The patient is experiencing pheochromocytoma with episodic catecholamine release
causing metabolic syndrome.
C. Excess ACTH from the pituitary adenoma drives bilateral adrenal hyperplasia and
cortisol overproduction, producing Cushing disease. ✓ CORRECT
D. The patient has Conn syndrome with aldosterone excess causing sodium retention
and striae formation.
, Correct Answer: C
Rationale: A pituitary adenoma secreting ACTH causes Cushing disease, which
stimulates the adrenal cortex to overproduce cortisol and creates the classic phenotype
of central obesity, striae, and hyperglycemia. Primary adrenal insufficiency causes
cortisol deficiency, not excess. Pheochromocytoma causes hypertension and sweating,
not striae. Conn syndrome produces hypertension and hypokalemia from aldosterone
excess without cushingoid features.
Question 5 of 50
A 38-year-old patient with autoimmune adrenalitis presents with hypotension,
hyponatremia, hyperkalemia, and hyperpigmentation of the skin creases and oral
mucosa.
A. The patient has secondary adrenal insufficiency from chronic exogenous
corticosteroid use.
B. Autoimmune destruction of the adrenal cortex has caused aldosterone and cortisol
deficiency, leading to sodium loss, potassium retention, and ACTH-driven melanocyte
stimulation. ✓ CORRECT
C. The patient has a pheochromocytoma causing episodic catecholamine release and
electrolyte disturbances.
D. Excess cortisol production from an adrenal adenoma has suppressed the
hypothalamic-pituitary axis.
Correct Answer: B
Rationale: Primary adrenal insufficiency from autoimmune adrenalitis destroys cortisol
and aldosterone production, causing hypotension, hyponatremia, and hyperkalemia,
while elevated ACTH stimulates skin hyperpigmentation. Secondary adrenal
insufficiency lacks hyperpigmentation and mineralocorticoid deficiency because ACTH
is low. Pheochromocytoma and excess cortisol syndromes do not present with
hypotension and hyperpigmentation.
Question 6 of 50
